Eph receptor deficiencies lead to altered cochlear function

MacKenzie A. Howard, Alma Rodenas-Ruano, Mark Henkemeyer, Glen K. Martin, Brenda L. Lonsbury-Martin, Daniel J. Liebl

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Ephrins and Eph receptors are a family of molecules that have been implicated in many developmental processes including neuronal network formation, guidance of cell migration, and axonal pathfinding. These molecules exhibit the ability to send bidirectional signals following ligand-receptor interactions resulting from cell-cell contacts. Gene-targeted knockout mice of B-class ephrins and Eph receptors have been shown to display phenotypic responses that correlate with anatomical defects. For example, disruption of the EphB2 receptor leads to defects of the vestibular system, including pathfinding abnormalities in efferent axons and reduced endolymph production. Such developmental distortions lead to deficiencies in ionic homeostasis and repetitive circling behaviors. The present study demonstrates that B-class ephrins and Eph receptors are expressed in cochlear tissues, suggesting that they may play some role in auditory function. To determine whether ephrins and Eph receptors have a functional role in the peripheral auditory system, distortion-product otoacoustic emission (DPOAE) levels, collected across a broad frequency range, were compared between groups of mice expressing different Eph receptor genotypes. In particular, EphB1 and EphB3 receptor knockout mice exhibited significantly diminished DPOAE levels as compared to wild-type littermates, indicating that these specific Eph receptors are necessary for normal cochlear function.

Original languageEnglish (US)
Pages (from-to)118-130
Number of pages13
JournalHearing Research
Volume178
Issue number1-2
DOIs
StatePublished - Apr 2003
Externally publishedYes

Fingerprint

EphA1 Receptor
Eph Family Receptors
Ephrins
Cochlea
EphB3 Receptor
EphB1 Receptor
Knockout Mice
EphB2 Receptors
Endolymph
Gene Knockout Techniques
Aptitude
Cell Communication
Cell Movement
Axons
Homeostasis
Genotype
Ligands

Keywords

  • Cochlea
  • Distortion-product otoacoustic emission
  • Eph receptor
  • Ephrin
  • Knockout mice

ASJC Scopus subject areas

  • Sensory Systems

Cite this

Howard, M. A., Rodenas-Ruano, A., Henkemeyer, M., Martin, G. K., Lonsbury-Martin, B. L., & Liebl, D. J. (2003). Eph receptor deficiencies lead to altered cochlear function. Hearing Research, 178(1-2), 118-130. https://doi.org/10.1016/S0378-5955(03)00068-6

Eph receptor deficiencies lead to altered cochlear function. / Howard, MacKenzie A.; Rodenas-Ruano, Alma; Henkemeyer, Mark; Martin, Glen K.; Lonsbury-Martin, Brenda L.; Liebl, Daniel J.

In: Hearing Research, Vol. 178, No. 1-2, 04.2003, p. 118-130.

Research output: Contribution to journalArticle

Howard, MA, Rodenas-Ruano, A, Henkemeyer, M, Martin, GK, Lonsbury-Martin, BL & Liebl, DJ 2003, 'Eph receptor deficiencies lead to altered cochlear function', Hearing Research, vol. 178, no. 1-2, pp. 118-130. https://doi.org/10.1016/S0378-5955(03)00068-6
Howard MA, Rodenas-Ruano A, Henkemeyer M, Martin GK, Lonsbury-Martin BL, Liebl DJ. Eph receptor deficiencies lead to altered cochlear function. Hearing Research. 2003 Apr;178(1-2):118-130. https://doi.org/10.1016/S0378-5955(03)00068-6
Howard, MacKenzie A. ; Rodenas-Ruano, Alma ; Henkemeyer, Mark ; Martin, Glen K. ; Lonsbury-Martin, Brenda L. ; Liebl, Daniel J. / Eph receptor deficiencies lead to altered cochlear function. In: Hearing Research. 2003 ; Vol. 178, No. 1-2. pp. 118-130.
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